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Quantum dots modulate intracellular Ca2+ level in lung epithelial cells
KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellulär biofysik. KTH, Centra, Science for Life Laboratory, SciLifeLab.
KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellulär biofysik. KTH, Centra, Science for Life Laboratory, SciLifeLab.
KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellulär biofysik. KTH, Centra, Science for Life Laboratory, SciLifeLab. AstraZeneca R&D, Sweden.
KTH, Skolan för teknikvetenskap (SCI), Tillämpad fysik, Cellulär biofysik. KTH, Centra, Science for Life Laboratory, SciLifeLab.
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2017 (Engelska)Ingår i: International Journal of Nanomedicine, ISSN 1176-9114, E-ISSN 1178-2013, Vol. 12, s. 2781-2792Artikel i tidskrift (Refereegranskat) Published
Abstract [en]

While adverse effects of nanoparticles on lung health have previously been proposed, few studies have addressed the direct effects of nanoparticle exposure on the airway epithelium. In this work, we examine the response of the pulmonary airway to nanoparticles by measuring intracellular Ca2+ concentration ([Ca2+](i)) in the Calu-3 epithelial layer stimulated by 3-mercaptopropionic-acid (3MPA) coated CdSe-CdS/ZnS core-multishell quantum dots (QDs). Simultaneous transient transepithelial electrical resistance (TEER) decrease and global [Ca2+](i) increase in Calu-3 epithelial layer, accompanied by cell displacements, contraction, and expansion, were observed under QD deposition. This suggests that a QD-induced global [Ca2+](i) increase in the Calu-3 epithelial layer caused the transient TEER decrease. The [Ca2+](i) increase was marked and rapid in the apical region, while [Ca2+](i) decreased in the basolateral region of the epithelial layer. TEER transient response and extracellular Ca2+ entry induced by QD deposition were completely inhibited in cells treated with stretched-activated (SA) inhibitor GdCl3 and store-operated calcium entry (SOCE) inhibitor BTP2 and in cells immersed in Ca2+-free medium. The voltage-gated calcium channel (VGCC) inhibitor nifedipine decreased, stabilized, and suppressed the TEER response, but did not affect the [Ca2+](i) increase, due to QD deposition. This demonstrates that the Ca2+ influx activated by QDs' mechanical stretch occurs through activation of both SA and SOCE channels. QD-induced [Ca2+](i) increase occurred in the Calu-3 epithelial layer after culturing for 15 days, while significant TEER drop only occurred after 23 days. This work provides a new perspective from which to study direct interactions between airway epithelium and nanoparticles and may help to reveal the pathologies of pulmonary disease.

Ort, förlag, år, upplaga, sidor
DOVE MEDICAL PRESS LTD , 2017. Vol. 12, s. 2781-2792
Nyckelord [en]
Calu-3 epithelial layer, quantum dot, intracellular Ca2+ concentration [Ca2+](i), transepithelial electrical resistance, cell movement
Nationell ämneskategori
Nanoteknik Farmaceutiska vetenskaper
Identifikatorer
URN: urn:nbn:se:kth:diva-206308DOI: 10.2147/IJN.S130136ISI: 000398663200001Scopus ID: 2-s2.0-85017256402OAI: oai:DiVA.org:kth-206308DiVA, id: diva2:1093367
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QC 20170505

Tillgänglig från: 2017-05-05 Skapad: 2017-05-05 Senast uppdaterad: 2018-01-13Bibliografiskt granskad

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Yin, HuijuanFontana, Jacopo M.Solandt, JohanJussi, Johnny IsraelssonXu, HaoBrismar, HjalmarFu, Ying

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Yin, HuijuanFontana, Jacopo M.Solandt, JohanJussi, Johnny IsraelssonXu, HaoBrismar, HjalmarFu, Ying
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Cellulär biofysikScience for Life Laboratory, SciLifeLab
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International Journal of Nanomedicine
NanoteknikFarmaceutiska vetenskaper

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